ACUTE RESPIRATORY DISTRESS

SYNDROME (ARDS)

Lungs: gas exchange

ANATOMY

PHYSIOLOGY

1.Inhale: diaphragm contracts downward:

lungs expand

vacuum effect: air will get in (oxygen)

2. Exhale: diaphragm relaxes

lungs relax

air will come out (carbon dioxide)

Air

Nostril (opening)

Nasal hair (filtrates dust and pollens)

Nasal cavity (releases mucus which has enzyme that kills pathogen)

Paranasal sinuses: frontal, ethmoid, sphenoid, maxillary ( warms and moist the air

Pharynx (nasopharynx, oropharynx, laryngopharynx)

Epiglottis (it closes when swallowing)

Larynx or voice box - (+) particles like food/ other than air; mechanism: coughing up
End of upper respiratory tract

Start of the lower respiratory tract

Trachea or windpipe

Carina

Primary: right and left bronchi (big bronchi)

Secondary and tertiary bronchi (small bronchi)

Bronchioles (smallest bronchi)

Alveoli (final destination of the air: preparing for gas exchange starts)

Alveolar wall is lined with pneumocytes which secretes surfactant; surfactant decreases surface tension to
keep the alveoli open and to prevent collapse of the alveolar wall

Alveolar macrophages will engulf if (+) particles and will move it up to the bronchi through mucociliary
escalator until to the pharynx

(-) particles/ clean air/ oxygen- ready for exchange

Alveolar wall

Basement membrane- separates air from the blood: blood-gas barrier

Pulmonary arteries which carries unoxygenated bloodcapillaries

Capillary which carries deoxygenated blood, carbon dioxide of the blood will be diffused in the alveoli

Carbon dioxide: breathe out

(-) particles/ clean air/ oxygen- will be diffused in the blood from capillaries

Oxygenated blood will be taken by the pulmonary vein and into the heart

PATHOPHYSIOLOGY
Common indirect cause: Sepsis
Burn
Common direct cause (lung): Aspiration
Pneumonia
Inhalation of toxic substances
Indirect and/ or direct cause will trigger inflammatory cells (white blood cells) to be active as a defense
mechanism of the body

Inflammation: 5 cardinal signs- redness, warmth, swelling, pain loss of function

Capillary membrane will be damaged/ ruptured, and will start the content/ fluid to leak into the alveolar sac.

ARDS three (3) phases:

1. Exudative - 24 hours post-injury regardless if direct or indirect cause
- “leakage”, fluid from capillary shifted into the alveolar sac, manifestation: pulmonary edema-crackles
- can also lead to damaged surfactant cells-alveolar will collapse/ atelectasis, manifestation: hypoxemia
Exudative- Hyaline membrane (accumulation of dead cells and proteins) will decrease the lung compliance
(less elastic), manifestation: Ventilation-Perfusion mismatch/ V/Q mismatch

V/Q mismatch- ventilation (airflow), perfusion (blood flow)

1. Exudative
Hallmark sign: Refractory hypoxemia (still hypoxemia even after high amount or level oxygen
administration) due to collapsed alveolar sac and hyaline membrane

Due to hypoxemia: increased RR- respiratory alkalosis (initially)- respiratory acidosis

2. Proliferative- 14 days post-injury

- “repair” but it will start to become fibrotic (thick)
- decreased lung compliance and hypoxemia will get worse

3. Fibrotic- 21 days post-injury

- poor prognosis due to its severity

Other signs:
 decreased LOC
 increased HR- compensatory mechanism
 respiratory failure
 cyanosis
 chest retraction
MANAGEMENT
1. Assess airway and monitor oxygen level of the client:
- SpO2 (oxygen saturation): 95-100%, for ARDS at least 90%
- PaO2 (partial pressure of oxygen): 75-100 mmHg, for ARDS at least 60 mmHg

2. Nutrition

3. Prevent pressure ulcer

2. Mechanical ventilation + Positive End- Expiratory Pressure (PEEP)

- To open collapsed alveoli sac and it will improve gas exchange
= PEEP titration: 10-20 cm H2O (high titration to compensate decreased lung compliance)
Complication:
• Increased thoracic pressure- heart will be affected/
compressed that can lead to hypotension
• Pneumothorax
• Subcutaneous emphysema- localized trap air under the skin

2. Mechanical ventilation
Settings:
Low pressure alarm- presence of leak due to possible
disconnection, tube displacement
High pressure alarm- pulmonary edema, pneumothorax, bronchospasm, secretions.

3. Prone position- better than supine in ARDS, heart and lungs will rest on the anterior part
4. Pulmonary artery wedge pressure
- ARDS- less than 18 mmHg
- Cardiac problem- greater than 18 mmHg

5. Corticosteroid to decrease inflammation

Acute Respiratory Failure (ARF)
ARDS can lead to ARF
Type 1: Acute Hypoxemic Respiratory Failure
➢ Inadequate oxygenation
Criteria:
• SpO2- less than 90 % (normal: 95% - 100 %)
• PaO2 (ABG analysis; partial pressure of
oxygen)- less than 60 mmHg (normal: 75- 100
mmHg)
Arterial Blood Gas Analysis
• Measures oxygen, carbon dioxide, ph
balance in the blood
• Site: radial Artery
Type 2: Acute Hypercapnic Ventilatory Failure
• ‘capnia’- carbon dioxide
Criteria:
• PaCO2- above 45 mmHg (normal 35- 45mmHg)
• pH- below 7. 35 (normal: 7.35- 7.45)
Causes of Acute Hypercapnic Ventilatory
Failure
• Brainstem injury/ head trauma
• Drug effect: opioid (morphine), benzodiazepine
(xanax)- decreases respiratory drive
• Chest trauma
• Neuromuscular conditions: Myasthenia gravis,
Amyotrophic Lateral Sclerosis, Guillain-Barre
Syndrome

Note: causes of Type 1/ Acute Hypoxemic

Respiratory Failure and Type 2/ Acute
Hypercapnic Ventilatory Failure can be both
applicable.

-It will depend on the manifestation whether

decreased oxygen (hypoxemic) or accumulation of
carbon dioxide (hypercapnia).

Causes of Acute Hypoxemic Respiratory

Failure
• ARDS
• High altitude
• Chest trauma
• Shock
• Pulmonary edema (common in left-sided heart
failure)
• Ventricular septal defect (VSD)
• Pneumonia